Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Effective renal plasma flow (ERPF) and linear cardiac output (aortic blood velocity) were measured in 15 patients who received halothane, enflurane or isoflurane in oxygen. All three agents caused a significant reduction in ERPF (P less than 0.05) and the effect was greater at 1.25 MAC than at 0.75 MAC. No significant difference was demonstrated between the agents. Linear cardiac output did not change significantly during the study, suggesting that the observed reduction in ERPF was not caused by cardiovascular depression.
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PMID:Effects of halothane, enflurane and isoflurane anaesthesia on renal plasma flow. 226 47

Using a rat model of incomplete cerebral ischemia the effects of isoflurane (iso) and methohexital (metho) were compared with those of 70% nitrous oxide controls (N2O). Two levels of incomplete cerebral ischemia were produced by right carotid occlusion plus hypotension for 30 min: moderate = 30 mmHg, FIO2 = 0.30; severe = 25 mmHg, FIO2 = 0.20. The iso doses (1 and 2 MAC) and metho doses (0.01 and 0.1 mg.kg-1.min-1) were tested at each ischemic level. These iso and metho doses were selected because without ischemia they produced similar decreases in cerebral oxygen consumption (CMRO2) compared with that produced in N2O controls. In the absence of ischemia, the electroencephalogram (EEG) was suppressed by 0.01 mg.kg-1.min-1 metho and 1 MAC iso and showed burst-suppression with 0.1 mg.kg-1.min-1 metho and 2 MAC iso. The EEG was further depressed by ischemia under all anesthetic conditions. Neurologic outcome was evaluated for 3 days following incomplete cerebral ischemia by using a graded deficit score (0 = normal, 5 = death associated with stroke). Following moderate ischemia all four anesthetic treatments improved outcome compared with N2O controls, but after severe ischemia only 2 MAC iso significantly improved outcome. Neurohistopathology was evaluated on a scale of 0 to 40, 24 h after ischemia. The neurohistopathology score was significantly improved by all four anesthetic treatments compared with N2O following moderate ischemia and was better with 2 MAC iso compared with 0.1 mg.kg-1.min-1 metho after both moderate and severe ischemia. These results show that both iso and metho improve outcome from cerebral ischemia compared with that associated with N2O, but only 2 MAC iso resulted in an improved outcome following severe ischemia. This difference in outcome between the two anesthetics may be related to greater neuronal depression with iso, which may occur with little difference in cerebral metabolic depression.
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PMID:Comparison of methohexital and isoflurane on neurologic outcome and histopathology following incomplete ischemia in rats. 229 37

Seventeen myasthenia gravis and seven control patients were studied mechano (MMG)- and electromyographically (EMG) during isoflurane/oxygen/air anaesthesia. In myasthenic patients the mean train-of-four ratio and neuromuscular block (by MMG) during 1.9 MAC isoflurane anaesthesia were 55 +/- 9% and 46 +/- 12%, respectively. The correlation between simultaneous MMG and EMG measurements was excellent (r2 = 0.933, P less than 0.001). The occurrence of HLA-B8 together with acetylcholine receptor antibodies seems to predispose myasthenic patients to a neuromuscular depression produced by isoflurane. Our current and prior results show that isoflurane possesses approximately twice as strong a neuromuscular blocking effect as halothane in myasthenic patients.
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PMID:Neuromuscular effects of isoflurane in patients with myasthenia gravis. 230 13

Development of an index of myocardial contractility that is both load independent and easily quantified in vivo has been a difficult task. Recently, three measures of contractile state have been advocated that appear to fulfill these requirements: the end-systolic pressure-length relationship (ESPLR), the ESPLR area, and regional preload recruitable stroke work (PRSW). Because the effects of halothane and isoflurane on these indices of contractility have yet to be studied, the purpose of this investigation was to compare the effects of these volatile anesthetics on contractile function as evaluated via these techniques in chronically instrumented dogs. Because autonomic nervous system tone substantially influences systemic hemodynamics in vivo, experiments were performed in the presence of pharmacologic blockade of the autonomic nervous system. Four groups comprised the 36 experiments that were performed with nine dogs. Following inhalational induction, the dogs were maintained on 1.5 MAC and 2 MAC of halothane or isoflurane. Pressure-length loops were generated after 1 h of equilibration using preload reduction via partial inferior vena caval occlusion or afterload augmentation by a phenylephrine infusion. The PRSW and ESPLR were then calculated, respectively. Slope and length intercept variables obtained from the ESPLR failed to significantly change from control with increasing levels of anesthetic depth despite substantial decreases in other indices of contractility. However, combination of slope and length intercept parameters into the ESPLR area model proved to be a sensitive and easily calculable measure of depressed myocardial function. Similarly, regional PRSW slope precisely reflected changes in contractile state when halothane (62 +/- 10 for control to 30 +/- 6 erg.cm-2.10(-3).mm-1 at 2 MAC) or isoflurane (83 +/- 14 for control to 55 +/- 8 erg.cm-2.10(-3).mm-1 at 2 MAC) were administered. The PRSW slope also demonstrated a significant difference in depressed contractility when equianesthetic concentrations of halothane and isoflurane were compared (63 +/- 7% of control with halothane versus 86 +/- 4% of control with isoflurane at 1.5 MAC; 50 +/- 5% of control with halothane versus 70 +/- 6% of control with isoflurane at 2 MAC). The ESPLR area also accurately demonstrated the differential depression in contractile function suggested by recent in vitro studies when equianesthetic doses of halothane and isoflurane were compared in vivo. Therefore, while ESPLR slope and length intercept variables fail as indices of myocardial contractility, ESPLR area and regional PRSW slope were shown to be useful indicators of contractile state in the conscious and anesthetized dog.
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PMID:Comparison of end-systolic pressure-length relations and preload recruitable stroke work as indices of myocardial contractility in the conscious and anesthetized, chronically instrumented dog. 201 75

The effects of two general anaesthetics, isoflurane--a volatile agent, and Althesin--a steroid preparation, were studied on the membrane electrical properties and spike activities of 64 neurons in in vitro slice preparations of neocortex excised from anterior cingulate and sensorimotor areas of guinea-pig brain. Spontaneous activity was depressed, and the thresholds for spikes evoked by intracellular injections of current pulses were increased in most neurons during applications of isoflurane in clinical concentrations (0.5-2.5 minimum alveolar concentration or MAC) and Althesin (15-100 microM). The MAC values are equivalent to 1-4% isoflurane in the gaseous phase. Applications in the higher ranges (1.5-2.5 MAC and 300-1500 microM) usually induced a small hyperpolarization (range, 3-8 mV) and an increase (10-30%) in input conductance. The repetitive spike firing evoked by current-pulse injections was inhibited and not uncommonly, abolished completely by an anaesthetic application. A striking feature in the actions of both agents on all neurons was the dose-dependent, reversible depression in amplitude and duration of the postspike afterhyperpolarizations (AHPs). These effects could not be attributed to anaesthetic induced changes in resting potentials, input conductances, or to the reduced number of evoked spikes. Bicuculline (50 microM) was applied concomitantly in 8 neurons with the anaesthetics to block Cl-conductances mediated by GABA-receptors that otherwise may "contaminate" the AHPs. In the presence of bicuculline, both anaesthetics produced a greater reduction in the amplitude and duration of the AHPs which are generated through Ca2+-mediated K+-conductance.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Postsynaptic depression induced by isoflurane and Althesin in neocortical neurons. 254 75

A decrease in synaptic excitation as well as an enhancement of neuronal inhibition in the central nervous system have been suggested as possible mechanisms of anaesthesia which we have investigated with intraneuronal recording techniques in neocortex. The effects of a volatile agent--isoflurane and a steroid preparation--Althesin, on excitatory and inhibitory postsynaptic potentials (EPSPs and IPSPs) evoked by epicortical electrical stimulation were investigated in in vitro slice preparations of anterior cingulate and sensorimotor cortices of guinea pig. Applications of isoflurane (0.5-2.5 minimum alveolar concentration or MAC) and Althesin (10-200 microM) induced a dose-dependent, reversible depression of EPSPs with EC50's of 1 MAC and approximately 50 microM respectively. In order to eliminate the possibilities of a shunting effect on EPSPs by the conductances involved in the concomitant IPSPs, a GABAA-antagonist (bicuculline) was applied together with the anaesthetics. With this IPSP blockade, both anaesthetics depressed the EPSPs and were effective in reducing the epileptiform activities evoked by bicuculline during the subpial stimulation. The IPSPs also were evoked during the blockade of K-conductances by internal Cs-applications in order that the effects of anaesthetics could be studied exclusively on the Cl-mediated GABAergic IPSPs. Both isoflurane (0.5-2.5 MAC) and Althesin (10-100 microM) depressed the IPSPs in a dose dependent manner. These investigations demonstrate that applications of isoflurane and Althesin depressed the excitabilities of neocortical neurons by interfering with synaptic excitation, possibly at pre- and postsynaptic sites, rather than by potentiating neuronal inhibition.
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PMID:Anaesthetic depression of excitatory synaptic transmission in neocortex. 255 15

alpha 2-Adrenergic agonists have been used as potent adjuncts to anesthesia and have anesthetic properties themselves. For this reason, we studied the effects of medetomidine, and isoflurane (1 MAC) on ventilatory drive in dogs. Six chronically tracheotomized mongrel dogs were studied during spontaneous ventilation. Arterial blood samples were analyzed for pH, PaCO2, and PaO2. Airway O2, CO2, N2, and isoflurane were continuously monitored using a mass spectrometer; respiratory rate was determined. The hypercapnic ventilatory response was assessed using the Read rebreathing technique. Control measurements were made under isoflurane anesthesia. Fifteen minutes after the medetomidine (20 ug/kg) was given and the isoflurane discontinued, all measurements were repeated. Isoflurane levels were 1.38 volume % during the isoflurane test period and had declined to 0.3 volume % by the time the medetomidine measurements were obtained. The slope of the CO2 response curve was significantly steeper after medetomidine (0.582 vs 0.269 1.min-1.mmHg), suggesting less respiratory depression when compared to the measurements under isoflurane. PaCO2 and endtidal CO2 were significantly lower in the medetomidine group. No other significant differences were found. Under these conditions, medetomidine (20 ug/kg) resulted in normal blood gas values with less depression of the hypercapnic response curve than under isoflurane anesthesia.
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PMID:The effects of medetomidine, an alpha 2-adrenergic agonist, on ventilatory drive in the dog. 257 Dec 80

The depressive effects of halothane (H) and isoflurane (I) on the same respiratory neuron were studied in cats. Using a tungsten microelectrode, activities of medullary inspiratory neurons were recorded around nucleus ambiguus. The number of spikes (Spike) of each respiratory cycle and inter-spike interval (ISI) were measured. At 1 MAC, in 9 units out of 11, Spike was significantly fewer with I than with H. In 2 units out of 11, Spike was not significantly different between H and I. These results indicate that each respiratory neuron shows different sensitivity to H and I at 1MAC concentration. With increasing depth of anesthesia, Spike showed a concentration-related depression. During the course of respiratory depression, the spikes were 75.9 (1MAC), 63.3 (1.5MAC), 48.0 (2MAC), 24.2 (2.5MAC), 5.0 (3MAC) with H, and 77.4 (0.5MAC), 51.9 (1MAC), 23.5 (1.5MAC) with I. These spikes were completely depressed at 3.5MAC in H and 2MAC in I. Both H and I increased ISI with increasing depth of anesthesia. The effects of H and I on the phrenic nerve discharges closely resembled their effects on the respiratory neurons. We conclude that the respiratory depression produced by I exceeds that produced by equal MAC of H.
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PMID:[A comparative study of the depressive effects of halothane and isoflurane on medullary respiratory neurons in cats]. 258 12

We studied the respiratory (R) and cardiovascular (CV) effects of 1.25 MAC halothane (H), isoflurane (I) and enflurane (E) in oxygen, delivered by the Jackson-Rees breathing system in 5 normothermic rats. Mean arterial pressure (MAP), heart rate (HR) were depressed after 30 minutes than stabilized after 2 hours anaesthesia regardless of the inhalational agent. Respiratory rate (RR) slowed down markedly unter I and E anaesthesia. Significant R depression was developed (PCO2 53.5 +/- 2.44 Torr) under E. Stabil metabolic condition was maintained. The R and CV changes caused by H and I were far less than changes produced by E. H or I is preferable to E for small animal anaesthesia with spontaneous breathing. Maintenance of constant temperature minimizes the CV and R disturbances.
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PMID:Comparison of respiratory and cardiovascular effects of halothane, isoflurane, and enflurane delivered via the Jackson-Rees breathing system in rats. New anaesthesia model for small animal surgery. 271 20

The effect of three different 1.2 MAC combinations of nitrous oxide (N2O) and enflurane upon glucose metabolism in the central nervous system was evaluated in male rats (n = 30). Anesthesia was induced with enflurane and N2O prior to tracheal intubation and mechanical ventilation. Physiologic variables (temperature, blood pressure, pH, PaO2, PaCO2, serum glucose, and hematocrit) were maintained within normal limits. Each rat was randomly assigned one of the following 1.2 MAC anesthetic regimens: 1) control--0% N2O/2.76% enflurane, 2) treatment 1--30% N2O/2.26% enflurane, or 3) treatment II--60% N2O/2.12% enflurane. Following anesthetic equilibration, an autoradiographic evaluation of local cerebral and spinal cord glucose utilization was performed. There were no differences in the physiologic data. As enflurane was partially replaced by an equivalent MAC fraction of N2O (0-30%), a heterogeneous activation of cerebral metabolism was observed in selected sensory input structures, and in components of the limbic system. The values tended to return to control when N2O was increased to 60% (and the enflurane was appropriately reduced). At all spinal cord levels, a homogeneous increase in metabolism was observed in both white and grey matter when enflurane was replaced by the 0-30% N2O change, with a return to control when the N2O was further increased from 30-60%. Thus, in rats, increasing the N2O concentration (while concurrently decreasing enflurane) produced a biphasic metabolic response. Metabolism was activated when N2O was increased from 0-30%, with a relative depression in metabolism when N2O was further increased from 30-60%.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Different 1.2 MAC combinations of nitrous oxide-enflurane cause unique cerebral and spinal cord metabolic responses in the rat. 271 12


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